Maternal periodontitis potentiates monosodium glutamate‐obesity damage on Wistar offspring's fast‐glycolytic muscle

• Published in: Oral diseases 2024-10, Vol.30 (7), p.4705-4720
• Main Authors: Costa, Liziane Nunes Conrad, Paula, Thayná Petry, Zazula, Matheus Felipe, Naliwaiko, Katya, Nassar, Carlos Augusto, Bertolini, Gladson Ricardo Flor, Torrejais, Marcia Miranda, Ribeiro, Lucinéia de Fátima Chasko, Costa, Rose Meire
• Format: Article
• Language: English
• Subjects: Adipose tissue; Animal models; Animals; Capillaries; chronic inflammatory diseases; Cytokines - metabolism; Female; foetal programming; Glycolysis; Gum disease; histological alterations; Male; Monosodium glutamate; Muscle, Skeletal - pathology; Neuromuscular junctions; Obesity; Obesity - complications; Obesity - metabolism; Offspring; Periodontitis; Periodontitis - complications; Periodontitis - metabolism; Periodontitis - pathology; Pregnancy; Prenatal Exposure Delayed Effects; Rats; Rats, Wistar; Sodium Glutamate - adverse effects; tibialis anterior; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 1354-523X; 1601-0825; 1601-0825
• DOI: 10.1111/odi.14890

Objective To evaluate the effects of magnifying the damage caused by obesity induced by monosodium glutamate, using a model of maternal periodontitis, on the structure of the anterior tibialis muscle of the offspring. Materials and Methods Twenty‐four female Wistar rats were divided into four experimental groups: control (n = 6), obese (n = 6), control with periodontitis (n = 6) and obese with periodontitis (n = 6). At 78 days of life, the rats were mated with males without any experimental intervention. The offspring of these rats (n = 1/L), at 120 days of life, were weighed and measured, then euthanized. Plasma was collected for analysis of cytokines IL‐6, IL‐10, IL‐17 and TNF‐α. Adipose tissues were collected and weighed, and the anterior tibial muscle was designated for histomorphological analyses (n = 6/group). Results Monosodium glutamate offspring showed significant muscle changes, such as a reduction in the size of fibres and neuromuscular junctions, and an increase in the nucleus and capillaries. However, all these changes were more expressed in monosodium glutamate‐obese with periodontitis offspring. Conclusion This leads us to suggest a magnifying effect promoted by periodontitis to the damage already well described by monosodium glutamate‐obesity, determined by low‐intensity inflammation, causing greater muscle damage.